Catheter Ablation in the Right Ventricular Outflow Tract Associated With Occlusion of Left Anterior Descending Coronary Artery.

Major vessel injury during right ventricular outflow tract ablation is not something widely recognized, and routine evaluation of the left anterior descending (LAD) artery location in relation to the septal right ventricle is not routinely performed. In the present article, we report a case of acute LAD occlusion after right ventricular outflow tract ablation and then illustrate the intimately close relationship of the LAD artery to the anterior septal site of the RVOT (approximately 2-3 cm under the pulmonic valve), using a combination of intracardiac echocardiography and 3-dimensional electroanatomical mapping recorded during a second case, in order to specifically point to the area at risk.

Feasibility, efficacy, and safety of radiofrequency ablation of atrial fibrillation guided by monitoring of the initial impedance decrease as a surrogate of catheter contact.

BACKGROUND: The initial impedance decrease during radiofrequency (RF) ablation is an indirect marker of catheter contact and lesion formation. We aimed to assess feasibility, efficacy, and safety of an ablation approach guided by initial impedance decrease. METHODS: A total of 25 patients with paroxysmal AF had point-by-point, wide antral pulmonary vein (PV) isolation. RF applications were aborted if a decrease of at least 5 Ω did not occur in the first 10 seconds; otherwise, ablation was continued for at least 20 seconds. Power was 30 Watts and reduced to 15-25 Watts on the posterior wall. RESULTS: A total of 28% of RF applications were terminated because of inadequate impedance decrease. The remaining lesions showed a median decrease of 7.6 Ω (IQR 5.0-10.7) at 10 seconds and median duration of RF lesions was 38 seconds. Note that, 100 PVs were isolated with 49 rings. PVI occurred before anatomic completion of the ablation ring of adequate lesions in 39/49 (80%) and concurrent with ring completion in 7/49 (14%). Additional lesions were required in 3/49 (6%) rings. After PVI, additional lesions were required to eliminate dormant conduction in 2/47 (4%) and pace-capture on the ablation line in 24/49 vein pairs (49%). During short-term follow-up, 3 nonfatal esophageal injuries and 2 late pericardial effusions occurred. During a mean follow-up of 431 ± 87 days, 21/25 patients (84%) remained free of recurrent symptomatic atrial arrhythmias. CONCLUSIONS: PVI guided by initial impedance decrease is feasible and results in PVI concurrent with or before completion of the ablation ring in 94% of patients. Single procedure efficacy after one year of follow-up was 84%. Near-term complications suggest that deeper lesions are created, indicating that further reduction of RF-power and duration is warranted.

Reentrant ventricular tachycardia originating from the periaortic region in the absence of overt structural heart disease.

BACKGROUND: In the absence of overt structural heart disease, most left ventricular outflow tract ventricular tachycardias (VTs) have a focal origin and are benign. We hypothesized that multiple morphologies (MMs) of inducible left ventricular outflow tract VT may indicate a scar-related VT that can mimic idiopathic VT. METHODS AND RESULTS: Of 54 consecutive patients referred for ablation of sustained outflow tract VT without overt structural heart disease, 24 had left ventricular outflow tract VT, 10 had MM VT, and 14 had a single VT (SM). The MM group were older (70.3±4.3 versus 53.9±15.9 years; P=0.004), had more hypertension (100% versus 29%; P=0.0006), and had longer PR intervals and QRS durations compared with the SM group. In contrast to the SM group, the MM group VTs had features consistent with reentry, including induction by programmed stimulation without isoproterenol, entrainment in some, and abnormal electrograms in the periaortic area. Periaortic region voltages suggested scar in the MM group, but not in the SM group. MRI in 2 MM patients was consistent with scar, but not in 10 SM patients. Longer radiofrequency applications were required in the MM group than in the SM group. At a median follow-up of 9.7 (3.0-32.0) months, recurrences tended to be more frequent in the MM group than in the SM group (70% versus 22%; P=0.07). CONCLUSIONS: VTs from small regions of periaortic scar can mimic idiopathic VT but are suggested by multiple VT morphologies and are more difficult to ablate. Whether these patients are at greater risk, as feared for other scar-related VTs, warrants further study.

Modeling of catecholaminergic polymorphic ventricular tachycardia with patient-specific human-induced pluripotent stem cells.

OBJECTIVES: The goal of this study was to establish a patient-specific human-induced pluripotent stem cells (hiPSCs) model of catecholaminergic polymorphic ventricular tachycardia (CPVT). BACKGROUND: CPVT is a familial arrhythmogenic syndrome characterized by abnormal calcium (Ca(2+)) handling, ventricular arrhythmias, and sudden cardiac death. METHODS: Dermal fibroblasts were obtained from a CPVT patient due to the M4109R heterozygous point RYR2 mutation and reprogrammed to generate the CPVT-hiPSCs. The patient-specific hiPSCs were coaxed to differentiate into the cardiac lineage and compared with healthy control hiPSCs-derived cardiomyocytes (hiPSCs-CMs). RESULTS: Intracellular electrophysiological recordings demonstrated the development of delayed afterdepolarizations in 69% of the CPVT-hiPSCs-CMs compared with 11% in healthy control cardiomyocytes. Adrenergic stimulation by isoproterenol (1 µM) or forskolin (5 µM) increased the frequency and magnitude of afterdepolarizations and also led to development of triggered activity in the CPVT-hiPSCs-CMs. In contrast, flecainide (10 µM) and thapsigargin (10 µM) eliminated all afterdepolarizations in these cells. The latter finding suggests an important role for internal Ca(2+) stores in the pathogenesis of delayed afterdepolarizations. Laser-confocal Ca(2+) imaging revealed significant whole-cell [Ca(2+)] transient irregularities (frequent local and large-storage Ca(2+)-release events, broad and double-humped transients, and triggered activity) in the CPVT cardiomyocytes that worsened with adrenergic stimulation and Ca(2+) overload and improved with beta-blockers. Store-overload-induced Ca(2+) release was also identified in the hiPSCs-CMs and the threshold for such events was significantly reduced in the CPVT cells. CONCLUSIONS: This study highlights the potential of hiPSCs for studying inherited arrhythmogenic syndromes, in general, and CPVT specifically. As such, it represents a promising paradigm to study disease mechanisms, optimize patient care, and aid in the development of new therapies.